Regulation of Carbapenemase Gene Conjugation in Clinical Isolates.

The purpose of this study is to raise awareness of the hazards of carbapenemase epidemics and provide theoretical support for preventing the spread of carbapenemase-producing organisms. A total of 893 non-duplicate strains were recruited from three major local hospitals. The carbapenemase genotype of each imipenem-resistant strain was analyzed.

Ibuprofen-mediated potential inhibition of biofilm development and quorum sensing in Pseudomonas aeruginosa.

Aims: Pseudomonas aeruginosa is one of the leading causes of opportunistic and hospital-acquired infections worldwide, which is frequently linked with clinical treatment difficulties. Ibuprofen, a widely used non-steroidal anti-inflammatory drug, has been previously reported to exert antimicrobial activity with the specific mechanism. We hypothesized that inhibition of P.

APOC3 promotes TNF-α-induced expression of JAM-1 in endothelial cell via PI3K-IKK2-p65 pathway.

Atherosclerosis is a chronic inflammatory disease with lipid accumulation. Apolipoprotein C3 (APOC3), which is an important regulator of human lipid metabolism, is associated with multiple vascular mechanisms in atherosclerosis and proinflammatory responses. We have previously reported that the expression of inflammatory cytokine TNF-α is elevated in human endothelial cells (HUVECs) after APOC3 treatment.

APOC3 induces endothelial dysfunction through TNF-α and JAM-1.

Background: The fatality rate for cardiovascular disease (CVD) has increased in recent years and higher levels of triglyceride have been shown to be an independent risk factor for atherosclerotic CVD. Dysfunction of endothelial cells (ECs) is also a key factor of CVD. APOC3 is an important molecule in lipid metabolism that is closely associated with hyperlipidemia and an increased risk of developing CVD.

Plasma miR-185 is decreased in patients with esophageal squamous cell carcinoma and might suppress tumor migration and invasion by targeting RAGE.

The receptor for advanced-glycation end products (RAGE) is upregulated in various cancers and has been associated with tumor progression, but little is known about its expression and regulation by microRNAs (miRNAs) in esophageal squamous cell carcinoma (ESCC). Here, we describe miR-185, which represses RAGE expression, and investigate the biological role of miR-185 in ESCC. In this study, we found that the high level of RAGE expression in 29 pairs of paraffin-embedded ESCC tissues was correlated positively with the depth of invasion by immunohistochemistry, suggesting that RAGE was involved in ESCC.

[The diagnostic value of quantitative measurement of a proliferation-inducing ligand mRNA in sputum samples from lung cancer patients].

Objective: To establish a real-time fluorescence quantitative polymerase chain reaction (RFQ-PCR) method for quantifying a proliferation-inducing ligand (APRIL) mRNA in sputum samples from patients with non-small cell lung cancer (NSCLC), and to evaluate its role in the diagnosis of NSCLC.

Methods: Seventy-one cases of NSCLC and 62 cases of benign pulmonary disease were enrolled in this study from August 2007 to May 2008 in Affiliated Hospital of Nantong University, Jiangsu. Sixty-five healthy volunteers served as the control.